The scourge of diabetes has led to an increase in the use of complementary and alternative medicine. The lack of regulation and control leads to the indiscriminate use of these herbals, with potential risk to patients.
Aim: This study evaluates the lipidaemic and hepatic status of type 2 diabetic rats treated with the polyherbal capsule glucoblock.
Methodology: A total of 35 male Wistar albino rats weighing between 120-220 g were used for this study. The rats were placed on high fat diet and diabetes was induced by a single intraperitoneal injection of freshly prepared streptozotocin (STZ) (45 mg/kg body wt). Fasting plasma glucose (FPG) was determined using the glucose oxidase method. Total Cholesterol (TC), Triglyceride (TG) and High Density Lipoprotein Cholesterol (HDL-C) were determined using enzymatic methods. Low Density Lipoprotein Cholesterol (LDL-C) was calculated using the Friedewald’s equation. Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) were determined using Reitman-Frankel method, while alkaline phosphatase (ALP) was determined using the colorimetric phenolphthalein method. Liver sections were stained using haematoxylin and eosin (H&E) staining technique, and phytochemical analysis was also done on the herbal capsule.
Results: The results show no significant differences in TC levels in all groups compared to the negative control. TG level was significantly higher in the diabetic control group when compared to the negative control. TG level in the singular treatment groups were significantly lower, but the combination group (glibenclamide + glucoblock) showed no significant difference compared to the diabetic control. The negative control had significantly higher HDL-C compared to the diabetic control and treatment groups. There were no significant differences in HDL-C levels in all the treatment groups, when compared to the diabetic control. The negative control had significantly lower LDL-C compared to the diabetic control and treatment groups. There were no significant differences in LDL-C levels in all the treatment groups, when compared to the diabetic control. ALT, AST and ALP levels were significantly higher in the diabetic control, but was significantly reduced to normal levels by the treatments. Liver sections of the negative control showed normal histoarchitecture. The diabetic control showed inflammation and fatty deposition. The treatment groups showed a nearly normal histoarchitecture, with fatty deposits.
Conclusion: High fat diet in combination with a sub-diabetic dose of streptozotocin produced significant diabetes in the Wistar rats with dyslipidaemia and elevated liver enzyme levels. The anti-diabetic treatments, glibenclamide and glucoblock did not correct the dyslipidaema caused by diabetes. However, the treatments had equipotent hepatoprotective effect and restored liver enzyme levels to normal as well as improving liver histology.